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Organ Systems III > OS III Exam IV > Flashcards

OS III Exam IV Flashcards

1
Q

Name the structures of the cortical part of the limbic system?

A

Cingulate, insula, parahippocampal gyrus

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2
Q

Name the structures of the subcortical part of the limbic system?

A

Hippocampus, amygdala, ventral striatum/nucleus accumbens

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3
Q

Describe the neuromodulatory pathways using norepinephrine and its key purpose.

A

NE: Projects from locus ceruleus to cortex (attention in stress)

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4
Q

Describe the neuromodulatory pathways using dopamine and its key purpose.

A

Dopamine: Projects from ventral tegmentum (midbrain) to PFC to basal ganglia (motivation)

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5
Q

Describe the neuromodulatory pathways using serotonin and its key purpose.

A

Serotonin: Raphe nucleus (medulla) to cortical areas

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6
Q

Describe the neuromodulatory pathways using acetylcholine and its key purpose.

A

Acetylcholine: Septum, nucleus basalis, and diagonal band of Broca project to thalamus and cortex.

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7
Q

Describe the location of the hippocampus.

A

Near the surface of the medial temporal lobe, bulges into the lateral ventricle.

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8
Q

Describe the connections of the hippocampus.

A

Afferents: cortex -> parahippocampal gyrus -> entorhinal cortex -> hippocampus

Efferents: Revers. hippocampus -> entorhinal cortex -> parahippocampal gyrus -> cortex.

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9
Q

Describe the overall functions of the hippocampus.

A

Encodes and consolidates episodic memories and projects them to wide areas of cortex.

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10
Q

What is declarative memory?

A

Episodic or semantic memory

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11
Q

Distinguish between episodic and semantic memory.

A

Episodic: autobiographical episodes or events, travel back in time.

Semantic: Non-contextual content of experience or knowledge about the world. Not accompanied with sense of self.

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12
Q

Describe the role of the hippocampus and vmPFC in forming and consolidating declarative memory.

A

Hippocampus consolidates memory and then project to cortex.

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13
Q

Where is declarative memory stored?

A

Cortex permanently.

Hippocampus (temporarily) consolidated.

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14
Q

Describe the stages of sleep.

A

REM (Rapid eye movement)

non-REM (includes slow-wave)

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15
Q

How do EEG correlate to sleep stages?

A

Non-REM: EEG waves increase amplitude and decrease frequency

REM: similar to waking, low amplitude and high frequency

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16
Q

Compare SWS and REM stages of sleep.

A

SWS earlier in sleep cycle, REM later in sleep cycle. Less SWS later in life.

SWS: inactive mind, active body
REM: active mind, inactive body

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17
Q

What are the pathways that maintain wakefulness?

A

Thalamus activated by cholinergic pontine pathways: pedunculopontine and lateral dorsal tegmental nuclei.

Cortex: Monoaminergic NE, serotonin, dopamine from basal forebrain.

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18
Q

How do you fall asleep?

A

VLPO inhibits via GABA and galanin all hypothalamic and brain stem nuclei.

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19
Q

How is sleep regulated by a circadian cycle?

A

Suprachiasmatic nucleus in hypothalamus reponds to light/dark. Through SPZ and DMH affects VLPO.
Cytokines TNF, IL disrupt pathway.

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20
Q

Describe how memory is consolidated in sleep.

A

Decrease Ach activates memory trace in hippocampus during SWS for transfer to neocortex. Slow waves allow oscillations between hippocampus and cortex without disruption of existing memory.

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21
Q

When does reactivation of memory occur during sleep?

A

SWS, decreased Ach

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22
Q

When are memories consolidated?

A

SWS

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23
Q

What role does the septum and diagonal band of Broca have in this?

A

Septum sets the theta rhythm, to avoid interference between simultaneous encoding and retrieval.

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24
Q

What sleep-wake conditions optimize memory consolidation?

A

Memory reactivated during SWS stabilizes memories.

Memory reactivated during REM enables “insight” or the discovery of hidden correlations.

Memory reactivated during wakefulness has the opposite effect, rendering memories labile and susceptible to modification.

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25
Q

How is memory consolidation affected in Alzheimer’s disease?

A

Degeneration of cortex, amyloid plaques around afferent axons, degeneration of hippocampus itself. Inability to consolidate short term into long term memories.

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26
Q

How is memory consolidation affected in bilateral hippocampectomy?

A

Loss of memory consolidation. Live in the present.

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27
Q

How are emotional experiences manifested?

A

1) ANS: BP, blood flow, digestive system
2) Behaviors: facial expression
3) Subjective feelings or drives: Love, fear, hate or hunger, thirst, lust, pain, pleasure.

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28
Q

What role does the amygdala play in expressing these emotional manifestations?

A

The central nucleus (CEN) of the amygdala mediates expression of innate and learned fear and anxiety.

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29
Q

What types of facial expressions do the amygdala respond to and why?

A

The amygdala responds best to ambiguity. Fearful or surprised faces achieve more response- unclear what the fear or surprise is about require vigilance.

Attention/vigilance required.

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30
Q

What is emotional memory?

A

Events associated or better remembered in an emotional context.

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31
Q

Describe conditioned fear and extinction and what brain areas generate them.

A

Fear conditioning is created through aversive events associated with certain stimuli.

This is never forgotten, merely overridden by the mPFC.

32
Q

How is the amygdala regulated in its expression of emotional responses?

A

It is regulated by the mPFC with input from the hippocampus to control response. E.g. Snake at the zoo.

33
Q

What does it mean that the amygdala retrieves emotional memories unconsciously?

A

The amygdala’s response to stimuli precedes your conscious perception of the stimuli mediated by auditory and visual association cortices.

34
Q

Compare memories of emotions vs emotional memories.

A

Memories of emotions is mediated by the medial temporal lobe. Whereas emotional memories are processed by the amygdala.

Retrieval of the memory by the medial temporal lobe enables conscious memory of emotional events, while retrieval by the amygdala allows expression of emotional reponses.

35
Q

How do high levels of NE and DA neuromodulation affect the relationship of prefrontal cortex and amygdala?

A

Inhibits PFC function

Strengthens fear conditioning in amygdala

36
Q

What is meant by top-down and bottom-up control of the amygdala?

A

Top-down: PFC
Bottom-up: sensory cortices

Normal: Top-down
In stress: Bottom-up

37
Q

What effects do lesions of the vmPFC/OFC and of the amygdala have on behavior?

A

vmPFC/OFC: inability to plan ahead, recognize sequence of actions, inhibit emotional tendencies from the amygdala

Amygdala: inability to recognize facial expressions (fear), to link past experiences to stimuli less aggression, to recognize objects, inappropriate sexual behavior.

38
Q

Describe the location and some of the functions of the insula.

A

Between frontal/temporal lobes.

Integrates bodily states into higher-order cognitive and emotional processes, connects with PFC, cingulate, and amygdala

39
Q

How does insula relate to the amygdala?

A

Anxiety.

Amygdala enhances insula’s anticipatory function.

40
Q

What the insula’s role in empathy?

A

Anterior insula (AIC) allows us to understand emotions in ourselves and others. Neural “as-if” construction.

41
Q

What the insula’s role in anxiety?

A

Hyperactivity of the insula is associated with anxiety disorders and fear conditioning.

Help with anticipation with respect to self to unexpected or novel stimuli.

42
Q

What is working memory?

A

The ability to maintain and update a few task-relevant representations in the mind; a mental sketch pad.

43
Q

Describe the dlPFC and its role in working memory.

A

Formulating, refining, and maintaining goals to organize behavior, solve problems, use working memory.

Important for sustained attention, screening distractions. Inhibits inappropriate impulses.

44
Q

What is the significance of the prefrontal cortex’s ability to sustain activity over long periods of time?

A

We can represent information that is not currently in our environment and process it with working memory.

Defines our conscious awareness. We have executive attention directed at stimulus.

45
Q

What is the role of NE and DA in maintaining working memory?

A

Facilitate working memory, generate alertness, increased signal/noise.

46
Q

What happens in the dlPFC if there is excess of NE and DA?

A

Disrupt working memory, reduced performance and distractibility.

47
Q

Contextually processed information is consolidated as memory into wide areas of ________.

A

Cortex: Prefrontal, temporal, parietal.

48
Q

What degenerates in narcolepsy?

A

Orexin/hypocretin pathways from lateral hypothalamus.

49
Q

How does increased Ach affect the hippocampus while awake?

A

Increases sensory input and encoding in hippocampus.

50
Q

Is the cholinergic activity greater when awake or when in REM sleep?

A

REM sleep

51
Q

What are some medications that diminish responses to facial expressions independent of their emotional valence?

A

Propranolol, B-adrenergic antagonist.

52
Q

How does NE affect the amygdala?

A

Enhances, reactivity and specificity (facilitated by cortisol)

53
Q

Compare lateral (executive) and medial (emotional) PFC connections.

A

Lateral PFC: sensory and motor cortices, executive function, intentional regulation of emotional behavior/experience.

Medial PFC: amygdala, AIC, hippocampus, reward aspect of tasks, emotional regulation

54
Q

How is the dlPFC affected in ADHD?

A

Underactive with weakened connections. Impaired executive function.

55
Q

What are the major constituents of the basal ganglia?

A

Caudate, Putamen, Nucleus accumbens, globus pallidus, subthalamic nucleus, substantia nigra, ventral tegmentum

56
Q

What is meant by the term striatum?

A

Caudate (includes nucleus accumbens) + Putamen

57
Q

Where are the basal ganglia located?

A

In the grey matter around the thalamus.

58
Q

Describe the source of dopamine neuromodulation for the striatum.

A

Substantia nigra, pars compacta, contains pigmented cells and projects to striatum.

59
Q

What is the corticostriate (CS) loop?

A

Anatomical loops that allow parallel processing of affective, cognitive, and motor components of behavior.

60
Q

What are the general functions of the direct and indirect pathways of CS loops?

A

Direct: neuronal circuit that functions to initiate and facilitate voluntary motor activity.

Indirect: inhibits muscles that would conflict with desired movement.

61
Q

What are the four known CS loops and what parts of the cortex do each of them involve?

A

Visual: temporal cortex, vlPFC
Motivational: anterior cingulate, orbito frontal cortex.
Executive: dlPFC
Motor/premotor: Primary, pre, and supplementary motor.

62
Q

What are the functions of each of the loops?

A

Visual: Integrates visual inputs into declarative and procedural learning of tasks.

Motivational: Regulates motivational-emotional aspects of behavior. Reward, feeding, addiction.

Executive: Internally generate movements, working memory, executive function

Motor/premotor: Programming and initiation of internally generated movements.

63
Q

Distinguish procedural memory from declarative and emotional memories.

A

Declarative: hippocampus-limbic
Emotional: amygdala
Procedural: cerebellum, basal ganglia

64
Q

What are the three aspects of procedural memory?

A

Implicit (unconscious), rigid (inflexible), procedural.

Also: category representation, action selection, instrumental/reward learning.

65
Q

What is the difference between declarative and procedural learning of visual categories?

A

Declarative learning: depends on processing in executive cortices (vmPFC, dlPFC) and hippocampus. Working memory.Skill attained in one trial. In a field of dots, which is the central one?

Procedural learning: depends on visual corticostriate loops, without awareness. No working memory. Point to middle dot in field of dots.

66
Q

What impact does dopamine neuromodulation have in action selection and instrumental/reward learning?

A

Dopamine to striatum selects responses that combine with other loops to form goal-directed activity. “Yeah, that’s it!”

Persistence of learning depends on synaptic modification by dopamine neurons.

67
Q

Distinguish between instrumental and reward learning.

A

Instrumental: Conditioned by association of a stimulus with a motor response. Externally drive.

Reward: Conditioned by association of a stimulus with a reward or desired outcome. Internally driven

68
Q

What is the difference in instrumental and reward learning outcomes?

A

Instrumental:
Reward:

69
Q

What are the general actions of addictive drugs on the motivational CS loop?

A

Mesolimbic system: enhance DA levels in the accumbens.

Imbalance between PFC and VTA acting on n. accumbens.

70
Q

What are the characteristics and causes of: chorea.

A

Characteristics: Involuntary jerky movements of face, tongue, limbs

Cause: lesions of striatum/cortex, underactivity of indirect pathways, loss of striatal GABA neurons to GP

71
Q

What are the characteristics and causes of: athetosis.

A

Characteristics: Writhing movements of limbs
Causes: Same loss of striatal GABA neurons seen in chorea

72
Q

What are the characteristics and causes of: hemiballismus

A

Characteristics: Flailing of limbs
Causes: Lesion of subthalamus (e.g. virus or CVA), reduces inhibitory control of thalamus.

73
Q

What are the characteristics and causes of: Parkinson’s disease.

A

Characteristics: Rest tremor, rigidity, inability to switch strategies, bradykinesia.

Causes: Degeneration of pigmented dopaminergic neurons in substantia nigra, SNpc

74
Q

How does pathology of dopamine neuromodulation fair in these conditions?

A

Dysregulation of indirect and direct pathway action on GPi neurons.

75
Q

What are the roles of the AIC and PIC?

A

AIC: Anterior Insula Cortex, integrates info from PIC, ACC, PFC, and amygdala. Subjective emotional awareness. Empathy!

PIC: Info regarding pain, temp, touch, itch, taste, visceral changes, and emotional touch

Organ Systems III (5 decks)

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